The growing literature conceptualizing mental disorders like posttraumatic stress disorder (PTSD) as networks of interacting symptoms faces three key challenges. Prior studies predominantly used (a) small samples with low power for precise estimation, (b) nonclinical samples, and (c) single samples. This renders network structures in clinical data, and the extent to which networks replicate across data sets, unknown. To overcome these limitations, the present cross-cultural multisite study estimated regularized partial correlation networks of 16 PTSD symptoms across four data sets of traumatized patients receiving treatment for PTSD (total N = 2,782). Despite differences in culture, trauma type, and severity of the samples, considerable similarities emerged, with moderate to high correlations between symptom profiles (0.43–0.82), network structures (0.62–0.74), and centrality estimates (0.63–0.75). We discuss the importance of future replicability efforts to improve clinical psychological science and provide code, model output, and correlation matrices to make the results of this article fully reproducible.
Major depressive disorder (MDD) is highly disabling and typically runs a recurrent course. Knowledge about prevention of relapse and recurrence is crucial to the long-term welfare of people who suffer from this disorder. This article provides an overview of the current evidence for the prevention of relapse and recurrence using psychological interventions. We first describe a conceptual framework to preventive interventions based on: acute treatment; continuation treatment, or; prevention strategies for patients in remission. In brief, cognitive-behavioral interventions, delivered during the acute phase, appear to have an enduring effect that protects patients against relapse and perhaps others from recurrence following treatment termination. Similarly, continuation treatment with either cognitive therapy or perhaps interpersonal psychotherapy appears to reduce risk for relapse and maintenance treatment appears to reduce risk for recurrence. Preventive relapse strategies like preventive cognitive therapy or mindfulness based cognitive therapy (MBCT) applied to patients in remission protects against subsequent relapse and perhaps recurrence. There is some preliminary evidence of specific mediation via changing the content or the process of cognition. Continuation CT and preventive interventions started after remission (CBT, MBCT) seem to have the largest differential effects for individuals that need them the most. Those who have the greatest risk for relapse and recurrence including patients with unstable remission, more previous episodes, potentially childhood trauma, early age of onset. These prescriptive indications, if confirmed in future research, may point the way to personalizing prevention strategies. Doing so, may maximize the efficiency with which they are applied and have the potential to target the mechanisms that appear to underlie these effects. This may help make this prevention strategies more efficacious.
Spousal bereavement can cause a rise in depressive symptoms. This study empirically evaluates 2 competing explanations concerning how this causal effect is brought about: (a) a traditional latent variable explanation, in which loss triggers depression which then leads to symptoms; and (b) a novel network explanation, in which bereavement directly affects particular depression symptoms which then activate other symptoms. We used data from the Changing Lives of Older Couples (CLOC) study and compared depressive symptomatology, assessed via the 11-item Center for Epidemiologic Studies Depression Scale (CES-D), among those who lost their partner (N = 241) with a still-married control group (N = 274). We modeled the effect of partner loss on depressive symptoms either as an indirect effect through a latent variable, or as a direct effect in a network constructed through a causal search algorithm. Compared to the control group, widow(er)s' scores were significantly higher for symptoms of loneliness, sadness, depressed mood, and appetite loss, and significantly lower for happiness and enjoyed life. The effect of partner loss on these symptoms was not mediated by a latent variable. The network model indicated that bereavement mainly affected loneliness, which in turn activated other depressive symptoms. The direct effects of spousal loss on particular symptoms are inconsistent with the predictions of latent variable models, but can be explained from a network perspective. The findings support a growing body of literature showing that specific adverse life events differentially affect depressive symptomatology, and suggest that future studies should examine interventions that directly target such symptoms.
Recent years have seen major developments in psychotherapy research that suggest the need to address critical methodological issues. These recommendations, developed by an international group of researchers, do not replace those for randomized controlled trials, but rather supplement strategies that need to be taken into account when considering psychological treatments. The limitations of traditional taxonomy and assessment methods are outlined, with suggestions for consideration of staging methods. Active psychotherapy control groups are recommended, and adaptive and dismantling study designs offer important opportunities. The treatments that are used, and particularly their specific ingredients, need to be described in detail for both the experimental and the control groups. Assessment should be performed blind before and after treatment and at long-term follow-up. A combination of observer- and self-rated measures is recommended. Side effects of psychotherapy should be evaluated using appropriate methods. Finally, the number of participants who deteriorate after treatment should be noted according to the methods that were used to define response or remission.
ObjectivesAlthough cognitive behaviour therapy (CBT) and pharmacotherapy are equally effective in the acute treatment of adult depression, it is not known how they compare across the longer term. In this meta-analysis, we compared the effects of acute phase CBT without any subsequent treatment with the effects of pharmacotherapy that either were continued or discontinued across 6–18 months of follow-up.DesignWe conducted systematic searches in bibliographical databases to identify relevant studies, and conducted a meta-analysis of studies meeting inclusion criteria.SettingMental healthcare.ParticipantsPatients with depressive disorders.InterventionsCBT and pharmacotherapy for depression.Outcome measuresRelapse rates at long-term follow-up.Results9 studies with 506 patients were included. The quality was relatively high. Short-term outcomes of CBT and pharmacotherapy were comparable, although drop out from treatment was significantly lower in CBT. Acute phase CBT was compared with pharmacotherapy discontinuation during follow-up in eight studies. Patients who received acute phase CBT were significantly less likely to relapse than patients who were withdrawn from pharmacotherapy (OR=2.61, 95% CI 1.58 to 4.31, p<0.001; numbers-needed-to-be-treated, NNT=5). The acute phase CBT was compared with continued pharmacotherapy at follow-up in five studies. There was no significant difference between acute phase CBT and continued pharmacotherapy, although there was a trend (p<0.1) indicating that patients who received acute phase CBT may be less likely to relapse following acute treatment termination than patients who were continued on pharmacotherapy (OR=1.62, 95% CI 0.97 to 2.72; NNT=10).ConclusionsWe found that CBT has an enduring effect following termination of the acute treatment. We found no significant difference in relapse after the acute phase CBT versus continuation of pharmacotherapy after remission. Given the small number of studies, this finding should be interpreted with caution pending replication.
We conclude that there is supporting evidence that preventive psychological interventions reduce the risk of relapse or recurrence in major depression.
Leading biological hypotheses propose that biological changes may underlie major depressive disorder onset and relapse/recurrence. Here, we investigate if there is prospective evidence for biomarkers derived from leading theories. We focus on neuroimaging, gastrointestinal factors, immunology, neurotrophic factors, neurotransmitters, hormones, and oxidative stress. Searches were performed in Pubmed, Embase and PsychInfo for articles published up to 06/2019. References and citations of included articles were screened to identify additional articles. Inclusion criteria were having an MDD diagnosis as outcome, a biomarker as predictor, and prospective design search terms were formulated accordingly. PRISMA guidelines were applied. Meta-analyses were performed using a random effect model when three or more comparable studies were identified, using a random effect model. Our search resulted in 67,464 articles, of which 75 prospective articles were identified on: Neuroimaging (N = 24), Gastrointestinal factors (N = 1), Immunology (N = 8), Neurotrophic (N = 2), Neurotransmitters (N = 1), Hormones (N = 39), Oxidative stress (N = 1). Meta-analyses on brain volumes and immunology markers were not significant. Only cortisol (N = 19, OR = 1.294, p = 0.024) showed a predictive effect on onset/relapse/recurrence of MDD, but not on time until MDD onset/relapse/recurrence. However, this effect disappeared when studies including participants with a baseline clinical diagnosis were removed from the analyses. Other studies were too heterogeneous to compare. Thus, there is a lack of evidence for leading biological theories for onset and maintenance of depression. Only cortisol was identified as potential predictor for MDD, but results are influenced by the disease state. High-quality (prospective) studies on MDD are needed to disentangle the etiology and maintenance of MDD.
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